This invention relates to an hsr (hypersensitivity-related) gene family and individual components thereof including its promoter and regulatory regions thereof, its coding region, its gene product; modifications thereto; applications of said gene, promoter region, regulatory region and coding region and modifications thereto; DNA constructs, vectors and transformed plants each comprising the gene or part thereof.
The hypersensitive reaction (HR) of higher plants is a local inducible response associated with disease resistance to a pathogen. This response is characterized by a rapid and localized necrosis of tissues invaded by an incompatible (avirulent or non-host) pathogen, which prevents further spread of the invading microorganism. Several defense genes whose products may intervene in this plant response have been extensively studied: they include enzymes of the phenylpropanoid pathway involved in the synthesis of antimicrobial phytoalexins, enzymes with hydrolyric activities, toxic compounds and cell wall proteins. In infected plants, these genes are induced around the necrosis, once it has developed, i.e. late during the HR. Moreover, most of them are also strongly expressed during compatible interactions leading to the disease of the plant, and for some of them, during the normal development of the plant. The lack of specificity of these defense genes as well as their activation in the late steps of the HR suggest that they may not account by itself for establishment of the complex inducible response that is the HR, but rather may accompany this reaction. To date, the molecular mechanisms leading from plant-pathogen recognition to development of the HR are not known. In the "gene for gene" hypothesis, the initial step of plant-pathogen recognition leading to resistance involves the putalive interaction between the products of a plant resistance gene and of the corresponding pathogen avirulent gene. Genetic studies indeed revealed that the outcome of many plant-pathogen interactions are determined through single dominant genes in both partners. Several rapid physiological changes have been also associated with the HR, such as electrolyte leakage, changes in respiration rates and more recently oxidative cross-linking of cell-wall proteins. However, in no case has a plant gene been described whose activation is specific or at least preferential during the resistance reaction, and precedes the development of the HR.
It is known that Pseudomonas solanacearum, a vascular bacterium, causes a lethal wilting of different plant species including Solanaceae. In this bacterium, a hypersensitive response (hrp) and pathogenicity gene cluster has been shown to control both the ability to elicit the HR on non-host plants and to cause the disease on host plants. In particular, hrp gene routants of P. solanacearurn have lost the ability to elicit an HR on tobacco plants. Recently, it was established that the hrpN gene of the hrp gene cluster of another bacterial pathogen, Erwinia amylovora, encodes a proteinaceous HR elicitor called harpin. This result confirms the important role of hrp genes in eliciting the HR. Upon infiltration of tobacco leaves by an HR-inducing incompatible isolate, six different gene families were characterized which are activated early during the interaction, before any necrosis of the leaf was detected. These genes which were not induced upon infiltration by an hrp-isolate differed by the accumulation levels of their transcripts during the incompatible versus the compatible interactions: the str (sensitivity-related) genes are expressed to a similar extent in both types of interactions, whereas the hsr genes are activated preferentially during the HR.